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Dementia, Renal Failure, and Brain Aluminum

ALLEN I. ARIEFF, M.D.; JERRY D. COOPER, M.D.; DEBORAH ARMSTRONG, B.A.; and VIRGINIA C. LAZAROWITZ, B.S.
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Presented in part at the Tenth Annual Meeting of the American Society of Nephrology, November 1977, Washington, D.C.

Grant support: Contract N01-AM-5-2204 from the Artificial Kidney/ Chronic Uremia Program, National Institute of Arthritis, Metabolism, and Digestive Diseases, National Institutes of Health; and the Medical Research Service of the Veterans Administration.

▸Requests for reprints should be addressed to Allen I. Arieff, M.D.; Veterans Administration Hospital (111J); 4150 Clement Street; San Francisco, CA 94121.


San Francisco, California


Ann Intern Med. 1979;90(5):741-747. doi:10.7326/0003-4819-90-5-741
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Dialysis dementia is a progressive and usually fatal neurologic syndrome occurring in patients on chronic hemodialysis. These patients may also have elevated levels of aluminum (Al+3) in the cerebral cortex. Possible relations between brain Al+3, increased Al+3 intake, and dementia were evaluated. Studies were done in seven groups of patients and five groups of experimental animals. In both normal dogs and rats and those with renal failure, oral Al+3 loading (Al[OH]3), resulted in significant increases of brain Al+3 (P < 0.01). In patients with renal failure, who were neither demented nor treated with dialysis, brain Al+3 was more than seven times normal (P < 0.01), whereas in patients with dialysis dementia, mean brain Al+3 was more than 15 times normal. However, the two groups were not significantly different. Brain Al+3 was also significantly elevated in patients who had either metastatic cancer or hepatic coma. Apparently brain Al+3 can be elevated as a consequence of Al+3 loading, renal failure, and abnormalities of the blood-brain barrier. It is most likely that dialysis dementia has multifactoral causation and is probably not caused by elevated brain content of Al+3 alone.

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